Pulmonary Effects Of Smoking Marijuana - Dissertation Example

Pulmonary Effects Of Smoking Marijuana Literature Review Marijuana scientifically referred to as Cannabis sativa is a dry hemp plant material that is often smoked like cigarette. Marijuana consists of an active ingredient called delta-9-tetrahydrocannabinol which plays a vital role in the destruction of the lungs and pulmonary systems of smokers. According to Winger et al (2004), delta-9-tetrahydrocannabinol is rapidly absorbed from the lungs and quickly bounds to the endogenous cannabinoid receptors within the central nervous system thus leads to psychoactive effects that users seek. Marijuana smoking is the commonest method of marijuana use and can either be rolled cigarette or through water filled pipe. Research show that many users of marijuana often inhale it as extremely hot fumes, usually to peak inspiration, and held as long as possible before being exhaled slowly. According to a study by Forrester et al (2012), this form of smoking has a greater impact on the pulmonary system because it predisposes the lung parenchyma to a greater damage than smoking of standard tobacco cigarettes. Research concerning the impacts of smoking marijuana have been done in the past and confirmed that the risk of regular smoking of marijuana is similar to those of regular tobacco smoking (Onaivi, 2006). There are many studies on the effects of tobacco on the respiratory system as well as certain diseases have been profiled and linked to tobacco. However, few studies have focused on the effect of marijuana on the pulmonary function. Hii et al (2008) investigated the effects of smoking marijuana upon pulmonary emphysema using a series of 10 patients consisting of ages between 32 and 50, two female and eight male. The participants were those who were presented over a period of 12 months in a respiratory unit showing new respiratory symptoms and those who admitted to be regular consumers of marijuana. The participants also exhibited the following symptoms on presentation including dyspnoea, pneumothorax and any kind of chest infection. In this study, high resolution CT shows variable sized, asymmetrical emphysematous bullae in the mid and upper zones. However, CT revealed normal CXR in four patients and normal functioning of the lung was normal in five patients. This study shows that marijuana smoking predisposes individual smokers to asymmetrical bullous disease mostly in normal CXR setting and function of the lung. The study also revealed that these pathological changes takes place at a younger age up to 2o years earlier compared to tobacco smokers (Hii et al, 2008). Current studies show that marijuana smoking is also associated with pulmonary fibrosis and lung bullae. As stated by Phan et al (2005), a case of twenty six years old Caucasian man presented with a history of exertional dyspnoea and dry cough for eight months had been smoking 10 cigarettes per day for 2 years and 10 pipes of marijuana per day for five years. The case report also indicated that the twenty six year old had no history of animal or occupational exposure, medications use or i.v. drugs use (Phan et al, 2005). The examination of this patient showed bilaterally reduced breath sounds that is an evidence of hyper-inflated lungs. This study also revealed that there was no cyanosis or clubbing and was a febrile. A radiograph examination of the patients’ chest also showed that there are widespread of opacities throughout the lungs. This case shows that marijuana smoking results into cystic changes which were particularly large in the lower zones in both lungs. There were extensive interstitial opacities throughout the lungs which included the upper mid and lower zones. The case presented above shows that marijuana can result into extensive damage onto lungs and the lower parts of the pulmonary system. As stated by Winger et al (2004), smoking marijuana often lead to a number of deformities; radiology, histology and lung function which all are related to heavy marijuana smoking. The combination of advanced pulmonary fibrosis, combination of lung bullae and heavy pigmented macrophage infiltration is unique (Phan et al, 2005). This study reveals the adverse effects of marijuana not only to the lungs but also to the other parts of the respiratory tract system. The destruction of marijuana by toxic chemicals resulting from marijuana is evident among both regular and long to short term smokers of marijuana. Milroy & Parai (2011) conducted an autopsy study which involved up to 13 marijuana smokers who suddenly died from accidental causes. This study revealed that the pigmented macrophages from marijuana infiltrated into the alveoli and interstitial of the lungs which is related to pulmonary fibrosis, emphysema and eventually chronic obstructive pulmonary disease (COPD) (ElSohly, 2007). The dose of marijuana also played a vital role in adverse effects that result into patients suffering COPD (Milroy & Parai, 2011). According to ElSohly (2007), the intensity of the infiltration of macrophages was closely related to the doses of marijuana smoked by the affected patients. This is because pigmented macrophages exhibit pulmonary toxicity hence causes tissue fibrosis. Other researchers have also confirmed these findings with very little variations with respect to lung damage. Milroy & Parai (2011) also reported six cases of young men who were significantly exposed to marijuana having lung bullae than those who were exposed to tobacco. In this respect, new findings are linking marijuana to not only severe cases of damage to the lower respiratory tract systems, but also to the pulmonary system (Onaivi, 2006). Emerging research reveal that smoking of marijuana is also linked to incidences of tuberculosis. Thu et al (2013) reported three cases of cavitating disease which were associated with common illicit smoking of marijuana using makeshifts and bong. As stated in this study the total number of positives contacts were 34 and out of 34 cases and among those sharing bong with an index case was associated with a six fold risk of transmission. As stated by, when tuberculosis is detected among young people in Australia, marijuana is most likely to be a possible risk factor. Even though this report is observational, it gives devastating effects of marijuana that includes predisposing individuals to other infectious diseases. While tuberculosis is caused by a strain of bacteria known as mycobacterium tuberculosis, it is important to note that the smoke of marijuana affects the body immunity system thus predisposes the body to other opportunistic infections (Rosenow & Camus, 2008). Several studies involving in vivo and in vitro research in both human and animal experiments, the smoke of marijuana compromises the natural defense mechanisms as well as the immunity of the body (Bedi et al, 2013). As stated by Onaivi (2006), smoking marijuana affects the tracheobronchial epithelial function thus interferes with clearance of mucus from the trachea. The smokers of marijuana also have their alveolar macrophages’ capacity to phagocytose Staphylococcus aureus compromised hence they produce reduced amounts of tumoour necrosis factor alpha, granulocyte-macrophage colony-stimulating factor and interleukin-6 (Bedi et al, 2013). It is these deficiencies that that could be predicted to improve the susceptibility to mycobacterial infection. This studies show that effects of marijuana is not only limited to the effects of the smoke itself, but the chemicals could interfere with body defense mechanism thus predisposes individuals to other infectious diseases of the pulmonary system. Gilbert et al (2013) compared the pulmonary effects of smoking marijuana and tobacco by qualifying the relative burden to the lungs of insoluble particulates as well as carbon monoxide from the smoke of the same quantities of tobacco and marijuana. Fifteen men who had smoked tobacco and marijuana habitually for more than five years had their blood tested for carboxyhemoglobin level before and after smoking. The mount of tar inhaled and deposited within the respiratory tract from tobacco and marijuana. This study found that unlike tobacco, smoking marijuana was associated with up to fivefold greater increment in the amount of carboxyhemoglobin level in the blood. The results of this study also revealed up to threefold increase in the amount of tar inhaled and retained within respiratory tract. In this regard, there are significant differences in smoking marijuana. Sarafian et al (2006) studied the effects of marijuana on the inflammation and atypia of airway epithelium accompanied by symptoms of chronic bronchitis. In this study, the investigators hypothesized that Delta 9-tetrahydrocannabinol (THC) which is the primary ingredient and psychoactive component of Marijuana is likely to results into the findings mentioned above by impairing function of the mitochondrion and impairing cellular energetics. The researchers tested this hypothesis by examining the particulate extracts from smoke from cigarettes’ smoke from tobacco and marijuana as well as placebo marijuana cigarettes for the effects on the mitochondrial function of theA549 cells in vitro. The results of this study reveal that the mitochondrion was destroyed by extracts from marijuana only. This shows that smoking of marijuana has the overall effects on airway epithelial cell energetics that is likely to results into adverse pulmonary consequences (Sarafian et al, 2006). This show that smoking marijuana is a health risk to pulmonary system and can result into pulmonary failure. References Bedi, G., Cooper, Z. D., & Haney, M. (2013). Subjective, cognitive and cardiovascular dose-effect profile of nabilone and dronabinol in marijuana smokers. Addiction Biology, 18(5), 872-881 ElSohly, M. A. (2007). Marijuana and the Cannabinoids. Totowa, N.J.: Humana Press Forrester, M., Kleinschmidt, K., Schwarz, E., & Young, A. (2012). Synthetic cannabinoid and marijuana exposures reported to poison centers. Human & Experimental Toxicology, 31(10), 1006-1011 Gilbert, C. R., Baram, M., & Cavarocchi, N. C. (2013). Smoking Wet. Texas Heart Institute Journal, 40(1), 64-67. Hii, S. W., Tam, J. C., Thompson, B. R., & Naughton, M. T. (2008). Bullous lung disease due to marijuana. Respirology, 13(1), 122-127 Milroy, C. M., & Parai, J. L. (2011). The histopathology of drugs of abuse. Histopathology, 59(4), 579-593. Onaivi, E. S. (2006). Marijuana and cannabinoid research: methods and protocols. New Jersey: Humana Press. Phan, T. D., Lau, K. P., & Li, X. (2005). Lung bullae and pulmonary fibrosis associated with marijuana smoking. Australasian Radiology, 49(5), 411-414. Rosenow, E. C., & Camus, P. (2008). Drug-induced and Iatrogenic Respiratory Disease. London: Hodder Arnold Sarafian, T. A., Habib, N., Oldham, M., Seeram, N., Lee, R., Lin, L., & ... Roth, M. D. (2006). Inhaled marijuana smoke disrupts mitochondrial energetics in pulmonary epithelial cells in vivo. American Journal Of Physiology. Lung Cellular And Molecular Physiology, 290(6), L1202-L1209. Thu, K., Hayes, M., Miles, S., Tierney, L., & Foy, A. (2013). Marijuana 'bong' smoking and tuberculosis. Internal Medicine Journal, 43(4), 456-458 Winger, G., Woods, J. H., & Hofmann, F. G. (2004). A handbook on drug and alcohol abuse: the biomedical aspects. New York: Oxford University Press. Read More